Role of trabecular bone in visibility of laminadura: A cross‑sectional radiographic study.

Aim: To determine the degree to which trabecular bone contributes to the radiographic visibility of laminadura (LD). Study Design: Human dry mandibles were obtained, and a series of radiographs were acquired in the premolar region. Radiographs taken were: (1) Before removal of any bone, (2) After removal of small amount of cortical bone at the apex of tooth, (3) Removal of trabecular bone, (4) Smoothing of endosteal surface of cortical bone. The radiographs were projected to a panel of six oral radiologists, and they were asked to judge the visibility of LD. Results: Chi‑square analysis revealed a significant radiographic difference between radiographs made initially and after removal of trabecular bone, cortical bone and smoothing the endosteal surface of cortical bone. Conclusion: There was statistically significant difference in the visibility of loss of LD when trabecular bone is lost. LD can be visible only if the endosteal surface of the cortical bone and trabecular bone is intact.

Unusual causes of fungal rhinosinusitis: A study from a tertiary care centre in South India.

Purpose: The frequency of mycotic infections of the nose and paranasal sinuses has been increasing over the past three decades. Apart from the common causes of fungal rhinosinusitis such as Aspergillus species and Penicillium species, there have been reports of rare and unusual fungi isolated from India and other countries. Objective: The objective of this study is to fi nd out the prevalence of fungal infections of the nose and paranasal sinuses caused by unusual fungal isolates at a tertiary care teaching hospital in South India. Materials and Methods: Duration of the study period was from April 2009 to March 2010. Specimens were collected from the nose and paranasal sinuses of all clinically and radiologically diagnosed cases of rhinosinusitis. All the clinical specimens were processed by standard methods for fungal culture. This included initial screening by 10% potassium hydroxide, inoculation of the specimen onto Sabouraud dextrose agar and incubation at 25°C and 37°C, followed by slide culture and other special techniques wherever necessary. Histopathological examination was also performed for the specimens. Results: A total of 60 specimens were received for fungal culture from cases of rhinosinusitis during the period, out of which 45 showed no growth. There were nine cases of Aspergillus fl avus, 1 each of Aspergillus fumigatus and Penicillium species. The rest four specimens grew rare fungal isolates, i.e. Acremonium sp., Scedosporium apiospermun, Cladosporium cladosporioides and Lasiodiplodia theobromae. Histopathological fi ndings were also positive for these four cases. Conclusion: Apart from the common causes, unusual fungal pathogens were isolated from cases of rhinosinusitis during the study period, which is in accordance with similar reports from other parts of India and some other countries.

Fatal cellulitis caused by Apophysomyces elegans.

A case of cellulitis of the left lateral side of the face caused by the zygomycete Apophysomyces elegans in a healthy male following a road traffic accident is reported. The contaminated soil was the source of fungus. Broad aseptate fungal hyphae were seen in the necrosed tissues. Extensive tissue debridement and treatment with amphotericin B were not successful in controlling the rapid invasion of the tissues by the fungus. Patient developed angioinvasion, severe cellulitis and finally succumbed to the infection three weeks after admission.

Familial hypodigoxinemic membrane Na(+)-K(+) ATPase upregulatory syndrome - relation between digoxin status and cerebral dominance.

A family with coexistence of hypotension, recurrent respiratory infection, motor tics, obsessive compulsive disorder, major depressive disorder, early onset osteoporosis, low body mass index, bulimia nervosa and healthy aging with longevity is described. The family members had hyposexual behavior, less tendency for spirituality, had no insomnia but a tendency towards increased somnolence, no addictive behaviour, had more bonding and affectionate behavior and were less creative with an average IQ. There was no vascular thrombosis, systemic neoplasm and neuronal degeneration in the index family. All members of the family were left hemispheric dominant. The level of serum digoxin, HMG CoA reductase activity and dolichol was found to be decreased in all with a corresponding increase in RBC Na(+)-K(+) ATPase activity and serum ubiquinone magnesium level. There was increase in tyrosine catabolites and a reduction in tryptophan catabolites in serum. Total and individual glycosaminoglycan fractions, carbohydrate residues of glycoproteins, glycolipids, activity of GAG degrading enzymes and glycohydrolases were decreased in serum. The concentration of RBC membrane total GAG and carbohydrate residues of glycoproteins increased while cholesterol : phospholipid ratio of membrane decreased. The activity of free radical scavenging enzymes were increased while the concentration of free radicals decreased significantly. The same biochemical patterns were observed in left hemispheric dominance as opposed to right hemispheric dominance. The significance of these findings in the pathogenesis of these disorders is discussed.

Inhibition of membrane Na+-K+ ATPase activity: a common pathway in central nervous system disorders.

OBJECTIVES: The study was conducted to assess the role of hypothalamic digoxin in neuropsychiatric and systemic disorders. A hypothesis regarding the central role of hypothalamic digoxin in neuroimmunoendocrine integration is proposed. METHODOLOGY: Blood samples from patients of CNS glioma, multiple sclerosis, systemic lupus erythematosis, subacute sclerosing panencephalitis, primary generalized epilepsy, Parkinson's disease, Down syndrome, AIDS dementia with neuropsychiatric features, syndrome X with multiple lacunar state, senile dementia, familial group (a family with familial coexistence of schizophrenia, Parkinson's disease, primary generalized epilepsy, malignant neoplasia, rheumatoid arthritis and syndrome X over three generations), schizophrenia and manic depressive psychosis were analysed for RBC membrane Na+-K+ ATPase, levels of digoxin and Mg++. RESULTS: Inhibition of RBC membrane Na+-K+ ATPase activity was observed in most cases along with increase in the levels of serum digoxin and decrease in the level of serum Mg++. CONCLUSION: The decreased Na+-K+ ATPase activity can be due to increased digoxin, which is a potent inhibitor of this enzyme. The inhibition of Na+-K+ ATPase can contribute to increase in intracellular calcium and decrease in magnesium, which can result in 1) defective neurotransmitter transport mechanism, 2) neuronal degeneration and apoptosis, 3) mitochondrial dysfunction, 4) defective golgi body function and protein processing dysfunction, 5) immune dysfunction and oncogenesis. The mechanism of how increased intracellular calcium and decreased magnesium can contribute to the above effects is discussed.

Changes in the isoprenoid pathway in syndrome X.

This study assessed the changes in digoxin and some other metabolites of the isoprenoid pathway in metabolic syndrome X presenting with multiple lacunar state. There was an increase in plasma HMG CoA reductase activity with a consequent increase in serum digoxin, which caused a reduction in RBC membrane Na+-K+ ATPase activity. There was an increase in serum tryptophan and its metabolites and a decrease in tyrosine and its metabolites. Serum magnesium was decreased with consequent alteration in the metabolism of glycosaminoglycans and glycolipids. Increase in dolichol, another product of the isoprenoid pathway resulted in alteration in glycoprotein metabolism. Changes in the composition of membrane glycosaminoglycans, glycoproteins and cholesterol:phospholipid ratio were also observed in this disorder leading to decreased lysosomal stability. Decrease in ubiquinone, another isoprenoid metabolite resulted in alteration in the free radical generation. Membrane Na+-K+ ATPase inhibition due to digoxin, altered membrane structure, increased tryptophan catabolites and decreased tyrosine catabolites can lead on to increased intracellular calcium and reduced intracellular magnesium which can account for the symptoms of syndrome X.

Hypothalamic digoxin and irritable bowel syndrome.

BACKGROUND: The hypothalamus produces an endogenous membrane Na+-K+ ATPase inhibitor digoxin that can modulate neurotransmitter transport and may play a role in hemispheric dominance. It can also modulate glycoconjugate synthesis and thus affect synaptic connectivity in the bowel wall. Digoxin could play a role in the genesis of irritable bowel syndrome (IBS). AIM: To study digoxin status in IBS and to correlate it with hemispheric dominance. METHODS: The isoprenoid pathway, tryptophan/tyrosine catabolic patterns and glycoconjugate metabolism were assessed in patients with IBS and in right hemispheric dominant/left hemispheric dominant/bihemispheric dominant individuals. RESULTS: The isoprenoid pathway was upregulated in IBS, with increased HMG CoA reductase activity (0.8 [0.07] vs 0.4 [0.06] in controls; p<0.01), serum digoxin (14.8 [1.0] vs 29.0 [1.2] ng/dL; p<0.01) and dolichol levels (63.8 [3.0] vs 120.3 [3.6] mg/dL; p<0.01). RBC membrane Na+-K+ ATPase activity (3.0 [0.2] vs 1.0 [0.1] microg/p/mg protein; p<0.01), serum magnesium (1.7 [0.1] vs 1.0 [0.1] mg/dL; p<0.01) and ubiquinone (86.4 [5.9] vs 39.8 [1.2] microg/dL; p<0.01) were reduced. There was increase in tryptophan catabolites and reduction in tyrosine catabolites. Serum total glycosaminoglycan and carbohydrate component of glycoproteins were increased in IBS. The activity of glycosaminoglycan degrading enzymes and glycohydrolases were increased. This pattern correlated with those obtained in right hemispheric chemical dominance. CONCLUSION: Hypothalamic digoxin and right hemispheric dominance could play a role in the genesis of irritable bowel syndrome.

Membrane Na+ K+ ATPase inhibition related dyslipidemia and insulin resistance in neuropsychiatric disorders.

There are several reports in literature implicating cholesterol metabolism in the pathogenesis of neuronal degenerations, oncogenesis, functional neuropsychiatric disorders and multiple sclerosis. Biosynthesis of cholesterol takes place by the isoprenoid pathway, which also produces digoxin, an inhibitor of membrane Na(+)-K+ ATPase. Inhibition of this enzyme results in intracellular Mg++ deficiency which can influence cholesterol metabolism. Digoxin also influences transport of tryptophan and tyrosine which are precursors of various neurotransmitters. Alterations in digoxin, membrane Na(+)-K+ ATPase and also in neurotransmitters have been reported in the disorders mentioned above. In view of this, serum lipid profile, activity of plasma HMG CoA reductase (the major rate limiting step in the isoprenoid pathway), RBC membrane Na(+)-K+ ATPase activity, serum Mg++ concentration, concentration of digoxin and concentration of serum neurotransmitters were studied in some neuropsychiatric disorders. The serum serotonin level was increased while that of serum dopamine and noradrenaline was reduced. Serum digoxin levels were high and RBC membrane sodium-potasium ATPase activity and serum magnesium were reduced. There was a reduction in HDL cholesterol and increase in plasma triglycerides (pattern similar to insulin resistance and syndrome X) in most of the disorders studied. The HMG CoA reductase activity was high, the serum total cholesterol was increased while RBC membrane cholesterol was reduced in most of the cases. The significance of increased digoxin with consequent inhibition of membrane Na(+)-K+ ATPase in relation to changes in cholesterol metabolism and insulin resistance type of dyslipidemia is discussed in this paper.

Hypothalamic digoxin and neural regulation of blood pressure and vascular thrombosis.

The isoprenoid pathway produces three key metabolites--digoxin (membrane sodium-potassium ATPase inhibitor and regulator of neurotransmitter/aminoacid transport), dolichol (regulates N-glycosylation of proteins) and ubiquinone (free radical scavenger). This was assessed in patients with essential hypertension, familial hypotension, acute coronary artery disease and acute thrombotic strokes. The pathway was also assessed in patients with right hemispheric, left hemispheric and bihemispheric dominance for comparison. In patients with acute coronary artery disease, acute thrombotic stroke, essential hypertension and right hemispheric dominance, there was elevated digoxin synthesis, increased dolichol and glycoconjugate levels and low ubiquinone and high free radical levels. There was also an increase in tryptophan catabolites, reduction in tyrosine catabolites, increase in cholesterol-phospholipid ratio and a reduction in glycoconjugate level of RBC membrane in this group of patients as well as in those with right hemispheric dominance. In patients with familial hypotension and left hemispheric dominance, the patterns were reversed. The role of a dysfunctional isoprenoid pathway and endogenous digoxin in the pathogenesis of essential hypertension and familial hypotension and in thrombotic vascular disease in relation to hemispheric dominance is discussed.

Surfactant protein-A: new insights into an old protein--II.

Pulmonary surfactant is a lipoprotein substance that lines the lungs and helps reduce surface tension. Surfactant associated protein-A (SP-A) is the most abundant non-serum protein in pulmonary surfactant. This complex glycoprotein aids in the synthesis, secretion and recycling of surfactant phospholipids, and facilitates the reduction of surface tension by surfactant phospholipids. Recent evidence has highlighted the role of SP-A in the innate immune system present in the lung. SP-A may play a major role in defense against pathogens by interacting with both infectious agents and the immune system. Factors that affect fetal lung maturation, e.g. gestational age and hormones regulate SP-A gene expression. Mediators of immune function also regulate SP-A levels. A number of lung disorders, including infectious diseases and respiratory distress syndrome are associated with abnormal alveolar SP-A levels. SP-A can no longer be called a lung-specific protein, since it has recently been detected in other tissues. In most species, SP-A is encoded by a single gene, however in humans it is encoded by two, very similar genes. Models for the structure of the human SP-A protein molecule have been proposed, suggesting that the mature alveolar SP-A molecule is composed of both gene products. The study of SP-A may provide information helpful in understanding disease processes and formulating new treatment modalities.

Surfactant protein-A: new insights into an old protein--Part I.

Pulmonary surfactant is a lipoprotein substance that lines the lungs and helps reduce surface tension. Surfactant associated protein-A (SP-A) is the most abundant non-serum protein in pulmonary surfactant. This complex glycoprotein aids in the synthesis, secretion and recycling of surfactant phospholipids, and facilitates the reduction of surface tension by surfactant phospholipids. Recent evidence has highlighted the role of SP-A in the innate immune system present in the lung. SP-A may play a major role in defense against pathogens by interacting with both infectious agents and the immune system. Factors that affect fetal lung maturation, e.g., gestational age and hormones, regulate SP-A gene expression. Mediators of immune function also regulate SP-A levels. A number of lung disorders, including infectious diseases and respiratory distress syndrome are associated with abnormal alveolar SP-A levels. SP-A can no longer be called a lung-specific protein, since it has recently been detected in other tissues. In most species, SP-A is encoded by a single gene, however in humans it is encoded by two, very similar genes. Models for the structure of the human SP-A protein molecule have been proposed, suggesting that the mature alveolar SP-A molecule is composed of both gene products. The study of SP-A may provide information helpful in understanding disease processes and formulating new treatment modalities.

Infant growth in relation to feeding practices in low income families.

A survey of feeding practices and measurements of weight, length and chest circumference of infants upto the age of 12 months and belonging to low income families of some selected villages at Pantnagar was carried out during 1987-88. The study revealed that as many as 83% of infants were exclusively breast fed up to the age of 6 months. In addition to being breast fed, 77% of infants between 9 and 12 months were also receiving semi-solids. Very small quantities of cereals, pulses, biscuits and fruits were reported to be the supplementary foods fed to infants. Animal milk diluted to varying degrees was fed as a supplement by some mothers and as a substitute by a few. Growth patterns of various feed types in terms of the anthropometric measurements were not found significantly different in different feeding practices. With reference to International standards (NCHS), it was seen that weight of only 25% of male and 55% of female infants fell in the normal range at the age of 3 months and this percentage declined from 3rd month to 12th month of age. Though the percentage falling in normal range was higher for length, the pattern of decline with the advancement in age was similar. This unsatisfactory growth performance of even those who received other foods along with breast milk is indicative of the fact that the quantity/quality of supplementary foods (along with other factors) were not sufficient to promote normal growth.